Freediving blackout

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Freediving blackouts fire-resistant blackouts or apnea blackouts are class hypoxic blackouts , loss of consciousness caused by brain hypoxia towards the end of the breath hold (freedive or dynamic apnea), when the swimmer does not need to experience the urgent need to breathe and have no other medical conditions that may have caused it. Can be triggered by hyperventilation just before diving, or as a consequence of reduced pressure on the climb, or a combination of these. Victims often establish diving practitioners breathing, fit, strong swimmers and have not experienced problems before. Blackout can also be called as syncope or fainting.

Divers and swimmers who pass out or gray under water during a dive will usually drown unless rescued and resuscitated in a short time. Freediving outages have a high mortality rate, and most involve men younger than 40, but are generally avoided. Risk can not be measured, but is clearly elevated by any degree of hyperventilation.

Freediving outages can occur on any dive profile: at a constant depth, on a climb from depth, or on the surface after the climb from depth and can be explained by a number of terms depending on the profile and depth of the dive in which consciousness is lost. Extinction during shallow dives differs from blackouts during ascent from deep dives in deep water blackouts triggered by depressurisation on ascending depths while shallow water shortages are a consequence of hypokapnia after hyperventilation.

Video Freediving blackout

Terminology

In this article constant pressure blackout and shallow water shortening refers to blackouts in shallow waters after hyperventilation and blackout and deep water blackouts refers to blackouts on the climb from the depths. Some free divers consider electrical outages on climbing to be a special condition or part of a shallow water extension but the underlying main mechanisms are different. This confusion is exacerbated by the fact that in the case of blackout on ascent, hypochapilation induced hypokapnia can also be a contributory factor even if depressurisation on ascent is a true precipitator.

Some scuba-dive curricula may apply different terms of shallow water blackouts and deep water outages ; deep water blackouts that are applied in the late stages of nitrogen narcosis while shallow water blackouts may be applied to blackouts from deep free dives. Narcotics Nitrogen usually does not apply to freediving because the diver is free to start and complete the dive with only one air lung and it has long been assumed that the free diver is not exposed to the pressure required long enough to absorb enough nitrogen. Where these terms are used in this way there is usually little or no discussion of the phenomenon of blackout does not involve depressurisation and its possible causes are variously associated with either depressurisation or hypocapnia or both. This problem may stem from the origin of the term latent hypoxia in the context of a series of fatal accidents, shallow water with the initial military, closed circuit rebreather equipment before the development of effective oxygen partial pressure measurements. In a very different context from dynamic apnea exercise careful consideration of the term is necessary to avoid potentially dangerous confusion between two phenomena that actually have different characteristics, mechanisms and preventive measures. The application of the term shallow water blackouts for deep diving and its relation to extreme sports has tended to mislead many static apnea practitioners and dive the distance of the dynamic apnea thinking that it does not apply to them even though the isobaric shallow water fight kills swimmers every year, often in the shallow pool.

The CDC has identified a series of voluntary consistent behaviors associated with accidental sinking, known as harmful breathing behaviors underwater; this is intentional hyperventilation, static apnea, and hypoxic training.

Other terms commonly associated with freediving outages include: Hyperventilation

Hyperventilation is inhaling more gas than necessary to compensate for metabolic consumption. There is a continuum between normal breathing and hyperventilation: "deep breathing", "breathing cleansing", or "breathing exercise" is a different name for hyperventilation. Some hyperventilation effects develop early in this process. There is a difference between filling the lungs with deep breaths to maximize available gas before diving, instead of taking deep breaths in a row; the latter will deplete carbon dioxide, without much effect on the supply of oxygen. This effect is illustrated in the graph in the shallow water blackout

Rescue breathing

Also known as hook breathing . This is a technique used by free diver on the surface to reduce the risk of surface blackouts. Partial partial execution, followed by a quick withdrawal; then the diver closes the airway and presses for a few seconds as if to cough. This behavior is repeated several times during the first 30 seconds or more on the surface. The goal is to keep the thoracic pressure slightly increased artificially increasing the partial pressure of the arterial oxygen or preventing it from falling in critical seconds until a newly oxygenated blood reaches the brain and thus prevents surface blackout. This is the same technique used by pilots during high-g-maneuvers, as well as by mountain climbers at high altitudes.

Lung packing

Technically known as glossopharyngeal insflation, pulmonary packaging or buccal pumping is a technique for inflating the lungs beyond their normal isobaric total capacity, which is used to delay lung compression at hydrostatic pressure, allowing depth which is bigger to achieve, and provides a slightly larger oxygen reserve for diving. After a full normal inspiration, the diver fills the mouth with air, with the glottis closed, then opens the glottis and forces air from mouth to lungs, then closes the glottis to hold it in the air. This is repeated several times. Lung packing can increase air volume in the lungs up to 50% of vital capacity. The pressure induced will reduce the volume of blood in the chest, which will increase the space available for air. The gas in the lungs is also compressed. A pressure of about 75 millimeters of mercury (100 mbar) has been reported. Lung packing has been associated with short-term haemodynamic instability, which may contribute to triggering a power outage.

Laryngospasm

Laryngospasm is an unintentional muscular contraction (spasm) of the vocal cords. This condition usually lasts less than 60 seconds, but in some cases it can last 20-30 minutes and leads to partial blocking of breath inspiration, while breathing expiration remains easier. This is a protective reflex against lung aspiration; this reflex can be triggered when the vocal cords or tracheal area below the vocal cords detect the entry of water, mucus, blood, or other substances. In the conscious subjects, there are some voluntary controls, which allow a relatively quick recovery of the airway.

Laryngospasm will relax with increased hypoxia, but the partial pressure of blood oxygen where this will occur is unknown (2006) and may be variable. Laryngospasm itself is usually not fatal if enough oxygen is available when the seizures relax.

Maps Freediving blackout

Mechanism

Minimal tissue and partial pressure of the oxygen vein that will maintain consciousness is about 20 millimeters of mercury (27 mbar). This is equivalent to about 30 milliliters of mercury (40 mbar) in the lungs. About 46 ml/min of oxygen is required for brain function. This is equivalent to a minimal arterial ppO ₂ of 29 millimeters of mercury (39 mbar) at 868 m1/min of cerebral flow.

Hyperventilation depletes the blood of carbon dioxide (hypocapnia), which causes respiratory alkylosis (increase in pH), and causes a leftward shift in the oxygen-hemoglobin dissociation curve. This results in a lower partial pressure of venous oxygen, which exacerbates hypoxia. A normally ventilated breath arrest usually breaks (from CO ₂) with more than 90% saturation away from hypoxia. Hypoxia produces respiratory impulses but is not as strong as hypercapnic respiratory impulses. It has been studied in altitude medicine, where hypoxia occurs without hypercapnia due to low ambient pressure. The balance between hypercapnic and hypoxic respiratory drives has genetic variability and can be modified by hypoxic training. This variation implies that predictive risk can not be reliably estimated, but pre-diving hyperventilation carries a definite risk.

There are three different mechanisms behind blackout in freediving:

Hypoxia induced duration occurs when the breath is held long enough for metabolic activity to reduce the partial pressure of oxygen sufficiently to cause loss of consciousness. This is accelerated by exertion, which uses faster oxygen or hyperventilation, which reduces the level of carbon dioxide in the blood which in turn can:
- increases the oxygen-hemoglobin affinity thereby reducing the availability of oxygen to the brain tissue towards the end of the dive (Bohr effect),
- suppresses the desire to breathe, making it easier to hold your breath to the point of darkness. This can happen anywhere.
Ascent-induced hypoxia is caused by a decrease in the partial pressure of oxygen when ambient pressure decreases as it rises. The partial pressure of oxygen at depth, under pressure, may be sufficient to maintain consciousness but only at that depth and not at reduced pressure in shallow waters above or on the surface.

The mechanisms for blackout on climb are different from hypokapnia-induced hypervigans that accelerate outages and do not always follow hyperventilation. However, hyperventilation will exacerbate risk and there is no clear line between them. Shallow water outages can occur in very shallow water, even in dry soil after hyperventilation and apnea but the effect becomes much more dangerous at the climbing stage of deep freedom. There is a lot of confusion around the phrases of shallow water outages and within and they have been used to refer to different things, or to be used interchangeably, in a circle of water sports different. For example, the term for shallow water blackouts has been used to describe blackouts on climbing because blackouts usually occur when the diver rises to shallow depths. For the purposes of this article there are two separate phenomena of shallow water blackouts and Blackout on ascending as follows:

Shallow water shortage

Otherwise, unexplained shutdowns under water have been associated with hyperventilation practices. Survivors of superficial water shortages often report using hyperventilation as a technique to increase the time they can spend underwater. Hyperventilation, or excessive breathing, involves breathing faster and/or deeper than the body demands naturally and is often used by divers in the mistaken belief that this will increase oxygen saturation. Although this appears to be intuitively true, under normal circumstances, the respiratory rate determined by the body alone leads to 98-99% oxygen saturation of arterial blood and the over-breathing effect on oxygen intake is minor. What really happened is different from the divers's understanding; These divers extend their dives by delaying the body's natural breathing mechanism, not by increasing the oxygen load. The mechanism is as follows:

The main drive for breathing is triggered by increased levels of carbon dioxide (CO ₂) in the bloodstream. Carbon dioxide accumulates in the bloodstream when oxygen is metabolized and needs to be disposed of as a waste product. The body detects carbon dioxide levels very accurately and relies on this as the main trigger for controlling breathing. Artificial hyperventilation depletes the concentration of carbon dioxide that causes a low carbon dioxide condition called hypokapnia. Hypocapnia reduces reflexive respiratory impulses, allowing respiratory delays and leaving divers susceptible to loss of hypoxic consciousness. For most healthy people, the first sign of low oxygen levels is grayout or unconscious: there is no body sensation that warns the diver from upcoming blackouts.

Significantly, the victim drowns subtly underwater without telling anyone the fact that there is a problem and is usually found at the bottom as shown in the staged image on the right. Survivors of superficial water shortages are usually confused as to why they faint. Pool rescue is trained to scan the bottom for the situation shown.

Hyperventilated breathing divers before diving increases their risk of drowning. Many sinks are not attributed to other causes resulting from shallow water shortages and can be avoided if these mechanisms are properly understood and the practice is eliminated. Shallow water shortages can be avoided by ensuring that the carbon dioxide levels in the body are normally balanced before diving and appropriate safety measures are applied.

High levels of hypocapnia are easily identified because they cause dizziness and tingling of the fingers. These extreme symptoms are caused by an increase in blood pH (alkalosis) after the reduction of carbon dioxide, which is necessary to maintain blood acidity. The absence of symptoms of hypokapnia is not an indication that the divertic carbon diver is within safe limits and can not be taken as an indication that it is safe to dive. Conservative breathing smugglers who have hyperventilated but stop doing it before the onset of these symptoms tend to have hypocapnic without realizing it.

Note that the drive for breathing is triggered by increased levels of carbon dioxide in the blood and not by oxygen depletion. The body can actually detect low oxygen levels but this is usually not seen before the blackout. Increasing levels of carbon dioxide in the blood, hypercapnia (opposite of hypokapnia), tend to make the body insensitive to carbon dioxide, in which case the body may depend on the level of oxygen in the blood to maintain its respiratory impulse. This is illustrated in a Type II respiratory failure scenario. However, in normal healthy people there is no subjective awareness of low oxygen levels.

Landing blackout

A blackout of climbing, or deep water blackouts, is a loss of consciousness caused by cerebral hypoxia as it rises from deep diving or diving, usually ten meters or more when the swimmer does not need to experience the urgent need to breathe and has no other obvious medical condition that may cause it. Victims are usually black close to the surface, usually within the top three meters, sometimes even when they break the surface and are often seen approaching the surface with no real difficulty just to sink. Very rarely occurs when power outages at the bottom or in the early stages of climbing; submerged divers in this stage are usually found to have water inhaled, indicating that they are conscious and yield to an uncontrollable urge to breathe rather than faint. Victims usually establish deep breath-hold diving practitioners, fit, strong swimmers and have not experienced any problems before. Blackout by this mechanism can occur even after emerging from the depth and breathing has begun if the inhaled oxygen has not reached the brain and can be termed as a surface blackout .

Partial pressure of oxygen in the air in the lungs controls the loading of blood oxygen. Critical PO ₂ of 30 millimeters of mercury (40 mbar) in the lungs will maintain awareness when breathing continues after breathing dives. It is about 4% oxygen in the lungs and 45% oxygen saturation of arterial blood. At 30 msw (4 bar), 2% of the volume of oxygen in the lung gas gave pO ₂ of 60 millimeters of mercury (80 mbar). At 10 msw (2 bar), for the same 2% oxygen, pO ₂ will be 30 millimeters of mercury (40 mbar), ie marginal. On the surface, the same 2% oxygen drops to 15 milliliters of mercury (20 mbar), ignoring the metabolic usage.

There are three factors that are considered to be involved: Voluntary breathing emphasis and rapid depression must exist, and hypo- ventilation induced by hyperventilation is present in many cases. Depressurisation on ascending is an explanation for the shallow depth of the climbing blackout but does not fully explain all cases unless accompanied by the underlying emphasis of the drive to breathe through self-induced hypocapnia through hyperventilation.

Voluntary breathing suppression. Deep water blackouts are sometimes attributed only to the ability of the diver practiced through training to suppress the urge to breathe. If living divers are aware that they have greatly suppressed the urge to breathe toward the end of the dive, there is a tendency not to seek further explanation. However, there are two problems with this as an explanation:

Even with high levels of training the hypercapnic drive to breathe is almost impossible to overcome; Swimmers usually suffer from inhaling water that is uncontrollable, cruel, and deep even when, intellectually, they know that doing so is fatal. It is a simple case of running out of air and sinking. Victims of a climbing blackout, if they have water in the lungs will at all have a limited amount in the bronchus that is consistent with the natural influx after death.

Survivors of intense deep water blackouts from below and above water show no sign of suffering associated with an uncontrollable urge to breathe and those who survived the blackout report no such distress. Many blackout events have been closely watched and even filmed because deep diving of apnea is a competitive event and deep diving requires great support of the crew both above and below the water. Anecdotes from healthy divers who hold their breath until unconscious without hyperventilation are difficult to prove and their ability, if any, is certainly very rare.

Rapid depressurisation. As the climbing outages occur as the diver approaches the surface of deep dives, depression is clearly present. Awareness depends on the minimum oxygen partial pressure in the brain rather than on the absolute quantity of the gas in the system. On the surface, air in the lungs is under 1 pressure atmosphere; at 10 meters, the water pressure doubled the air pressure in the 2nd lung of the atmosphere. Diving with recreational breath can often reach below 20 meters, competitive divers can go deeper, and record "free-limit" diving exceeds 200 meters since 2007. Ten meters is easily achieved by a reasonably fit and competent swimmer. Most people lose consciousness when the partial pressure of oxygen in their lungs, usually 105 millimeters of mercury (140 mbar) falls below about 30 millimeters of mercury (40 mbar). A ppO ₂ of 45 millimeters of mercury (60 mbar) at ten meters would be tolerable for divers at that depth, but would likely result in a blackout between four meters and a surface when ambient pressure reduction carries a partial pressure of oxygen at below the limit. S.Miles calls this latent hypoxia. Although comfortable enough at the bottom of the diver may actually be trapped by latent hypoxia, and do not realize that it is now impossible to ascend safely, but is likely to pass out without warning just as he approaches the surface.

Self-induced hypokapnia. Hyperventilation that causes hypokapnia and loss of proper urge to breathe is the mechanism behind superficial water shortages. Many deep water practitioners hold their breath using hyperventilation in order to extend their base time, so this mechanism is also relevant for deep water blackouts in these cases. If the divers is hyperventilated, the mechanism is essentially for shallow water shorts, but hypoxia is delayed by pressure at depth and occurs only when the pressure falls when it comes to the surface. This explains why these fainted divers do so close to the surface on their way up and why they may not feel the urgency to breathe at all; suitable, the free diver rising from the deep diving could faint without any warning.

Surface blackout
Surface blackouts occur only after the diver exhales on the surface, and may occur before, during or after the first breath. When divers exhale, there is usually a reduction in intrathoracic pressure, which is exacerbated by inhalation efforts, which can further compromise the partial pressure of oxygen in the alveolar capillaries, and after a small time lag, the supply of oxygen to the brain. Exhaling also reduces the buoyancy of divers and increases the risk of drowning as a result of power outages. A decrease in intrathoracic pressure may also reduce cardiac output for this period and thus further compromise with the cerebral oxygen supply. The delay between breathing and oxygenated blood reaching the brain can exceed 15 seconds. Competent freediving security monitors observe the diver for at least 30 seconds after surfacing. Rescue breathing may reduce the risk of surface blackouts during critical periods after surfacing.
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Consequences
The usual consequence of a power outage, if the diver's air duct is unprotected, sinks. A diver who passes out and immediately returns to the surface will usually regain consciousness within seconds. While divers are still unconscious underwater, they are at high risk of drowning. The time between loss of consciousness and death varies greatly depending on a number of factors but can be as little as 2 ¹/₂ minutes.
An unconscious diver loses voluntary body control, but still has a protective reflex that protects the airway. One is spasm of the larynx, which closes the larynx to prevent water from entering the lungs. After some time, the laryngospasm will relax and the airway will open. If the diver has reached the surface and the face of the diver is stored above the water, when laringospasm relaxes spontaneous breathing will often continue.
If the diver is still under water when laryngospasm is relaxed, the water will enter the airway and may reach the lungs, which will lead to complications even if resuscitation is successful. Secondary drowning can occur as a result.
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Differential diagnosis
The sudden and unexpected death of the swimmer, without an accidental drowning sequence, can be difficult to assume a particular cause. The possibilities may include pre-existing organic heart disease, pre-existing cardiac electrical abnormalities, epilepsy, hypoxic blackout, murder and suicide. Diagnosis may have significant legal consequences.
Careful recording of observed events may increase the likelihood of a correct diagnosis. Hypoxic outbreaks may have been seen to have hyperventilation before dives, and usually blackouts will occur shortly after submersion, often without surfacing, and usually close to the surface. The victim was later found unconscious or dead at the bottom of the water. The witness account can be useful in diagnosing the cause and in the resuscitation and treatment of the victim.
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Risk
The risk of a freediving blackout is unknown because there is currently no strict data on freediving outages. However, the estimated, average, annual casualties associated with blackout freedivers over a ten-year period in a population of around 135,000 divers in nine countries are 53 per year, or one in 2,547. The total number of deaths seems to remain unchanged in recent years but it is not possible to calculate the mortality rate due to variables such as the number of dives or the unknown diver population. Risks also differ across cultures and diving practices. For example, about 70% of Italian divers who regularly compete in national and international spearfishing competitions have at least one blackout while Japanese divers Ama have low levels of blackouts because they follow conservative diving profiles, limit the duration of diving by up to one minute, rest between diving and making some short dives than fewer ones.
Experienced dives have special risks because of their practiced ability to suppress carbon dioxide induced induces to breathe. Some argue that the highest risk may be for medium skilled divers who practice hard and do not recognize their limits.
Where in-breathing diverters are observed to use timely hyperventilation and informed advice may save their lives but experience suggests that divers are reluctant to change their practice unless they have a very clear understanding of the mechanism of the process.
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Management

Avoidance and prevention
Hyperventilated breathing divers before diving increases their risk of drowning. Many sinks are not attributed to other causes resulting from shallow water shortages and can be avoided if these mechanisms are properly understood and the practice is controlled or eliminated. Increased advocacy to increase public awareness of risk is one of the few ways available to try to reduce the incidence of this problem.
Shallow water shortages can be avoided by ensuring that the carbon dioxide levels in the body are normally balanced before diving and appropriate safety measures are applied. The following precautions are recommended by some organizations:

Divers should be weighed to provide positive buoyancy on the surface even after breathing. Weight should be discarded if in trouble.

Before diving, the diver should relax and allow the blood oxygen and carbon dioxide to reach equilibrium. Divers should breathe normally in preparation for diving, and allow normal breathing triggers to determine respiratory rates to ensure carbon dioxide levels are within safe limits. The last pre-dive breath should have been for full inspiratory capacity.

If excited or anxious about dives, divers should be more careful to stay calm and breathe naturally when adrenaline (epinephrine) can cause hyperventilation without the diver being aware.

When the urge to breathe comes near the end of the dive, the diver must immediately appear and breathe. Breathing recovery should not be necessary, but it may not be dangerous.

Divers should not dive alone. Diving in a friend's partner, one to observe, one for diving, allows the observer to try to save in the event of a power outage. Safety dives should always have good ventilation and be ready to go rescue immediately.

Diving should be in the depth of both divers. However, this still depends on the buddy who pays attention to the problem in time, and is able to reach a depressed diver, under emergency pressure.

Once surfaced, the diver's condition should be monitored for at least 30 seconds.

Couples should know how to recognize and manage power outages.

High levels of hypocapnia are easily recognized because they cause dizziness and tingling of the fingers. This extreme symptom is caused by an increase in blood pH (alkalosis) after subtraction of CO ₂, which is necessary to maintain blood acidity. The absence of symptoms of hypocapnia is not an indication that carbon dioxide levels of divers are within safe limits and can not be taken as an indication that it is safe to dive. Conservative breathing smugglers who have hyperventilated but stop doing it before the onset of these symptoms tend to hipokapnik without realizing it.
Direct banning of hyperventilation training and breath-taking exercises in the pool may reduce or prevent the occurrence of blackouts in the pool, but may result in activities performed elsewhere where there may be less supervision and a higher risk of death. Supervision by someone who is not involved in the activity and familiar with risk and management blackout is the preferred choice.
The incident analysis shows that the lifeguard at the pool can prevent most of the accidents by watching the young male swimmers practicing hyperventilation and swimming underwater.
Recognition
Recognizing the problem in time to help is crucial; divers will not see any symptoms and depend on your dive buddy or surface support team to gain recognition. The blackout indicators for searching on divers include:

Stop swimming for no apparent reason.

Start sinking.

Arms or legs are weak.

Eyes return or close.

The head falls forward.

Tissue or seizures.

Rescue
Rescue requires a competent diver on site to recover unconscious divers onto the surface, or prevent them from drowning in case of a surface blackout. This requires the safety diver to know the status of the diver in time to react effectively. Unconscious freedivers must be brought to the surface with a minimum delay. There is no risk of excessive blood pressure injury, and the airway should be secured if possible to prevent aspiration. Masks are adequate protection from the nasal passages if in place, and the hands can be used to cover the mouth and hold it closed.
Once it appears, make sure the air channel is open. Masks can be removed at this point. Divers can spontaneously continue breathing. The general response time after shallow dives is 3 to 10 seconds, increasing up to 10 to 30 seconds for deep dives. If the diver starts breathing and regain consciousness spontaneously, they should be monitored until they get out of the water.
If the diver does not spontaneously continue breathing, respiratory rescue (artificial ventilation) is indicated. Victims should be removed from the water immediately and basic life support provided until expert assistance is available.
First aid and medical care
When first aid and medical care is needed, it is to drown.
The initial resuscitation followed the standard procedure for drowning. Response and respiratory examination is done with people who are horizontally supine. If unconscious but breathing, the recovery position is correct. If not breathing, rescue ventilation is required. Drowning can produce a panting pattern of apnea while the heart is still beating, and ventilation alone is enough, since the heart may be basically healthy, but hypoxic. The order of breath-breath circulation should be followed instead of starting with compression, since the underlying problem is lack of oxygen. Five initial breaths are recommended, since initial ventilation may be difficult because water in the airways can interfere with effective alveolar inflation. After that a two-breath sequence and 30 chest compressions are recommended, repeated until vital signs are re-established, rescuers can not continue, or continued life support is available.
Source of the article : Wikipedia